Novel expression of luteinizing hormone/chorionic gonadotropin receptor gene in rat prostates

“…However, there is a large body of evidence for the presence of such receptors in various extragonadal organs (8)(9)(10). Although the level of LHR expression in the extragonadal sites is generally low (15,31,32) and functional data are sparse, there are some rather convincing in vitro findings of hCG-stimulated signal transduction and biochemical responses in non-gonadal sites, in particular in the uterus. The signaling involved in these actions invariably differs from the cAMP-mediated action of LH in gonads (11,(33)(34)(35).…”

Section: Figurementioning

confidence: 98%

Fertility in luteinizing hormone receptor-knockout mice after wild-type ovary transplantation demonstrates redundancy of extragonadal luteinizing hormone action

Pakarainen

Zhang²,

Poutanen³

et al. 2005

Journal of Clinical Investigation

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The luteinizing hormone receptor (LHR), mainly expressed in gonads, is essential for normal reproduction. However, numerous recent studies have also demonstrated LHR expression in multiple extragonadal reproductive and nonreproductive tissues. Although some effects of luteinizing hormone (LH) or its agonist, human chorionic gonadotropin, have been shown in extragonadal sites, their physiological significance remains open. In the present study, we have addressed the function of the extragonadal LHR using LHR-KO mice (LuRKO mice), in which the ovaries of prepubertal mice were orthotopically replaced with pieces of WT ovary using similarly transplanted WT mice as controls . Most ovarian transplants attained normal endocrine function in both groups of mice, as demonstrated by normal age at vaginal opening, estrous cycles, and sexual behavior. Both the LuRKO and WT mice repeatedly became pregnant (9/16 vs. 16/20 after first mating; difference not significant) and delivered similarly sized litters, which grew normally after birth, indicating normal lactation. In conclusion, fertility is restored in LuRKO mice by transplantation of WT ovarian tissue. This is achieved in the absence of extragonadal LHR expression, which indicates physiological redundancy for such receptor sites. IntroductionThe regulatory functions of the 2 gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), form the cornerstone of normal fertility. In addition to earlier studies on hypophysectomized animals, immunoneutralization of gonadotropins or gonadotropin-releasing hormone (GnRH), and treatment with GnRH analogs, more recent studies on targeted inactivation of the gonadotropin subunit and receptor genes have specifically demonstrated the need of proper function of LH, FSH, and their receptors for the maintenance of female reproduction (1-7).Quite unexpectedly, a number of studies have recently reported the presence of the common LH and human chorionic gonadotropin (hCG) receptor (LHR) in a variety of extragonadal tissues, including the uterus, oviduct, cervix, placenta, mammary gland, sperm, certain areas of the brain, and many others (8-11). Many of the findings were made on human tissues, but similar observations have been reported on a number of other mammalian species, including baboons, bovines, pigs, rats, and mice (9,(12)(13)(14)(15). On the basis of these observations, a shift in the old paradigm that gonadotropins only have gonadal actions has been proposed (8). A number of extragonadal actions for LH/hCG have been suggested, including effects on brain development and sexual behavior, regulation of

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“…Mature sperm are stored in distal cauda epididymis [1,2]. Although androgens are very important [1,2,7], other regulatory molecules are also involved in controlling epididymal functions [1,2,[8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Epididymal Phenotype in Luteinizing Hormone Receptor Knockout Animals and Its Response to Testosterone Replacement Therapy1

Lei

Zou

Mishra

et al. 2003

Biology of Reproduction

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Previous studies reported that epididymis contains functional LH receptors. The LH receptor knockout mice, which have epididymal phenotypes, gave us an opportunity to test the hypothesis that testosterone replacement alone may not be sufficient to reverse phenotypes to wild-type epididymis. The morphological phenotype in knockout animals includes a decrease in luminal diameter of the proximal and distal caput and cauda epididymis, the absence of clear and halo cells in the epithelial lining, a decrease in the height of principal cells and the number of cells containing cilia, a decrease in cilia length, and a change from basal to central location of nuclei in the principal cells. The biochemical phenotype includes a decrease in periodic acid-Schiff reaction product, reflecting the glycogen and glycoprotein synthesis and secretion, a decrease in androgen receptor (AR) and estrogen receptor (ER)beta, and an increase in ERalpha levels. Twenty-one-day testosterone replacement therapy in 30-day-old knockout animals reversed some, but not all, morphological and biochemical phenotypes. Those that did not reverse include luminal diameters of proximal and distal caput and cauda epididymis, the percentage of ciliated principal cells in caput epididymis, and nuclear AR localization. In summary, while our results reaffirm that androgens are important for normal epididymal morphology and function, they indicate that LH could be required for certain facets of epididymal morphology and/or function.

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Novel expression of luteinizing hormone/chorionic gonadotropin receptor gene in rat prostates

Cited by 35 publications

References 20 publications

Effects of pituitary hormones on the prostate

Effects of pituitary hormones on the prostate

Fertility in luteinizing hormone receptor-knockout mice after wild-type ovary transplantation demonstrates redundancy of extragonadal luteinizing hormone action

Epididymal Phenotype in Luteinizing Hormone Receptor Knockout Animals and Its Response to Testosterone Replacement Therapy1

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